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Effect of pleiotrophin on glutamate‐induced neurotoxicity in cultured hippocampal neurons
Author(s) -
Asai Hitomi,
Morita Shoko,
Miyata Seiji
Publication year - 2011
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1802
Subject(s) - neurotoxicity , glutamate receptor , pleiotrophin , hippocampal formation , chemistry , neurotoxin , neuroscience , microbiology and biotechnology , propidium iodide , biology , biochemistry , programmed cell death , receptor , growth factor , apoptosis , toxicity , organic chemistry
Pleiotrophin (PTN) is a secreted heparin‐binding cytokine that signals diverse functions, including lineage‐specific differentiation of glial progenitor cells, axonal outgrowth and angiogenesis. Neurotoxicity mediated by glutamate receptor is thought to play a role in various neurodegenerative disorders. In the present study, we examined the effect of PTN on the neuronal viability of hippocampal neurons in vitro by using the immunostaining of MAP2 and permeability of propidium iodide. PTN significantly prevented glutamate‐induced neurotoxicity when hippocampal neurons were treated with PTN after the glutamate stimulation. PTN significantly promoted glutamate‐induced neurotoxicity, when cells were incubated with PTN before and after the glutamate stimulation. Thus, the effect of PTN on the neuronal viability of hippocampal neurons largely depends on the timing of the treatment of PTN. The treatment of PTN promoted dendrite‐specific expression of MAP2, indicating that PTN stabilizes microtubule system at dendrites. The data suggest that PTN may be relevant to be concerned with glutamate‐induced neurotoxicity of hippocampal neurons. Copyright © 2011 John Wiley & Sons, Ltd.